The endothelial function can be modified by environmental toxics as lead; microalbuminuria is a marker of endotelial disfunción and reflects early and generalized alteration of it. Microalbuminuria, is a marker of renal risk, and a powerful indicator of cardiovascular risk mortality. Objective: evaluate if low level lead treatment (0.5 ppm) produces microalbuminuria and if it undergoes modifications with time of exposition. Wistar rats, with 0.5 ppm lead acetate in the drink water were included. The animals were separated in three groups according to the time of treatment in: 6, 9 and 12 months; the fourth group constituted of control with water ad libitum. Laboratory: Plombemia by atomic absorption, determination of microalbuminuria by turbidimetric method (latex) of Biosystems. Results: rats controls average of microalbuminuria: 2.41± 0.79 mg/dl. Rats treated during 6 months, 9 months and 12 months: 3.25 ± 1.05 mg/dl, 6.17± 1.24 mg/dl and 27.4 ± 15.78 mg/dl respectively. When comparing the group control with each one of the treated groups significant differences were observed in all the cases, p<0.03 (Mann Whitney), comparing with the control, a greater difference was found in the treated group during 12 months with p<0.01 (ANOVA). A low dose of lead exposition produces microalbuminuria, which progresses in relation to the time of metal exposition. This work fortified the hypothesis of lead role in cardiovascular diseases origin.